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Related Concept Videos

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PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

Updated: Jul 2, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

VALD-3 Induces GSDME-Dependent Pyroptosis via ROS/JNK/Bax Pathway in Triple-Negative Breast Cancer Cells.

Xuhui Zhao1, Xuhong Pan2, Weijie Ma1

  • 1Department of Oncology, Gansu Provincial Hospital, Lanzhou, 730000, Gansu, P.R. China.

Biochemical Genetics
|July 1, 2026
PubMed
Summary
This summary is machine-generated.

VALD-3, a novel compound, effectively combats triple-negative breast cancer (TNBC) by selectively inducing pyroptosis, a programmed cell death, in cancer cells. This targeted approach inhibits tumor growth and offers a promising new avenue for TNBC treatment.

Keywords:
Caspase-3GSDMEPyroptosisTNBCVALD-3

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis and limited treatment options.
  • Existing therapies for TNBC often lack specificity and efficacy, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anticancer effects of VALD-3, a Schiff base ligand derivative, on breast cancer cells.
  • To elucidate the mechanism of VALD-3-induced cell death, focusing on pyroptosis in TNBC.

Main Methods:

  • VALD-3 treatment of TNBC and ER+ MCF-7 cells.
  • Assessment of cell viability, pyroptotic features, reactive oxygen species (ROS) levels, JNK phosphorylation, and mitochondrial pathway activation.
  • Analysis of caspase-3 activation and gasdermin E (GSDME) cleavage.

Main Results:

  • VALD-3 exhibited potent cytotoxicity against TNBC cells, more so than ER+ MCF-7 cells.
  • VALD-3 selectively induced pyroptosis in TNBC cells, characterized by cell swelling and inflammatory cytokine release.
  • The mechanism involved increased ROS and JNK phosphorylation, leading to mitochondrial apoptosis pathway activation, caspase-3 activation, and GSDME-dependent pyroptosis.

Conclusions:

  • VALD-3 effectively eradicates TNBC cells through GSDME-dependent pyroptosis.
  • The ROS/JNK/Bax-mitochondrial apoptosis pathway is crucial for VALD-3-induced pyroptosis.
  • VALD-3 represents a potential novel therapeutic agent for triple-negative breast cancer.